Gonda Tamas A, Tu Shuiping, Wang Timothy C
Division of Digestive and Liver Diseases, Department of Medicine, Irving Cancer Research Center, Columbia University, New York, NY, USA.
Cell Cycle. 2009 Jul 1;8(13):2005-13. doi: 10.4161/cc.8.13.8985. Epub 2009 Jul 11.
Chronic inflammation often precedes or accompanies a substantial number of cancers. Indeed, anti-inflammatory therapies have shown efficacy in cancer prevention and treatment. The exact mechanisms that turn a wound healing process into a cancer precursor are topics of intense research. A pathogenic link has been identified between inflammatory mediators, inflammation related gene polymorphisms and carcinogenesis. Animal models of cancer have been instrumental in demonstrating the diversity of mechanisms through which every tumor compartment and tumor stage may be affected by the underlying inflammatory process. In this review, we focus on the interaction between chronic inflammation, tumor stem cells and the tumor microenvironment. We summarize the proposed mechanisms that lead to the recruitment of bone marrow derived cells and explore the genetic and epigenetic alterations that may occur in inflammation associated cancers.
慢性炎症常常先于或伴随大量癌症出现。事实上，抗炎疗法已在癌症预防和治疗中显示出疗效。将伤口愈合过程转变为癌症前体的确切机制是深入研究的课题。炎症介质、炎症相关基因多态性与致癌作用之间已确定存在致病联系。癌症动物模型有助于证明潜在炎症过程可能影响每个肿瘤区室和肿瘤阶段的机制多样性。在本综述中，我们重点关注慢性炎症、肿瘤干细胞与肿瘤微环境之间的相互作用。我们总结了导致骨髓来源细胞募集的推测机制，并探讨了炎症相关癌症中可能发生的遗传和表观遗传改变。
